Bhatia Yashpreetsingh A.

IV BDS
ROLL NO : 3
Diabetes Mellitus and its Oral
Manifestations
Introduction
Diabetes mellitus is a metabolic disease
characterized by abnormally elevated blood
glucose levels (hyperglycemia) and dysregulation
of carbohydrate, protein, and lipid metabolism.


Epidemiology
Prevalence is similar in both males and females.
Incidence rises as the population ages and
prevalence of obesity increases.
An average medical practice will have between
60 and 70 diabetic individuals for every 1000
patients and 50% of these will be undiagnosed.
- US prevalence data
Classification Characteristics
Type 1 DM (Insulin-dependant
DM, formerly juvenile diabetes)
Beta cell destruction, leading to
absolute insulin deficiency.
Immune mediated.
Idiopathic.
Type 2 DM (Non insulin-
dependant DM, formerly adult-
onset diabetes)

Insulin resistance with relative insulin
deficiency.
Other specific types of DM
Heterogeneous group in which etiology
is estb. or partially known.
Genetic defects of beta cell function
Genetic defects in insulin action
Diseases of exocrine pancreas
Endocrinopathies
Drugs or chemically induced, etc.
Gestational DM
Any degree of glucose intolerance with
onset or 1
st
recognition during
pregnancy.
Pathophysiology
The primary feature of hyperglycemia results
from:-
1. A defect in Insulin secretion from pancreas or
2. Resistance of bodys cells to insulin action, or
both.

Normally,
Breakdown of carbohydrate
Blood Glucose
Insulin secretion
Insulin binds to specific cell receptors and
glucose enters cell
Blood Glucose level
Insulin secretion
If insulin secretion is decreased, glucose entry
in cells is inhibited resulting in hyperglycemia.
A rise in insulin secretion may cause blood
glucose levels to become very low i.e.
hypoglycemia.
Excess glucose is stored in liver in form of
glycogen that acts as reservoir for future use.
Glycogen is converted into glucose via
glycogenolysis elevating blood glucose levels
and providing the needed cellular energy
source.
Liver also produces glucose from fatty acids
and amino acids through process of
gluconeogenesis.
Insulin decreases blood glucose levels while
Glucagon, GH, catecholamines, thyroid
hormones and glucocorticoids all increase blood
glucose levels.
Type 1 Diabetes mellitus
Type 1 DM is characterized by idiopathic
autoimmune destruction of beta cells leading
to absolute insulin deficiency.
It occurs before the age of 25 yrs in 95% of
affected persons but may occur at any age.
M=F
Risk increased by family history of Type 1 DM,
gluten entropathy (coeliac disease), or
endocrine diseases.
Two subclasses:
1) Immune mediated autoimmune destruction of
beta cells in pancreatic islets.
2) Idiopathic

Type 1 DM patients depend on exogenously
administered insulin for survival. They are
highly susceptible to diabetic ketoacidosis.
Diabetic Ketoacidosis
Glucose cant enter cells and remains in bld.
stream.
Fat lipolysis(to meet cellular demands)
Glycerol and free fatty acids released.
Glucose Ketones
Increased Ketones in body fluids & decreased H
+

ion

Electrolyte loss,dehydration, alteration in HCO
3
-

buffer system
Diabetic Ketoacidosis

Coma and Death.
Converted to
If untreated
Type 2 DM
It is most common type 90 to 95 % cases.

Characterised by insulin resistance in peripheral
tissues and defective insulin secretion by the
pancreatic beta cells.

Individuals are overweight and mostly adults.

MODY: Maturity Onset Diabetes of Young.

Etiology:
Genetic predilection, advancing age, obesity
and lack of exercise.

Pathophysioliogy:
1) Peripheral resistance to insulin, especially in
muscle cells.
2) Increased production of glucose by the liver.
3) Insulin secretory defect of the beta cells.

These patients are generally resistant to Diabetic
ketoacidosis.
Clinical presentation
Type 1 - sudden onset
Type 2 - often remains undiagnosed for years.
Charecteristic triad of Polydypsia, polyphagia and
polyuria
Unexplained weight loss, poor wound healing,
blurred vision, gingival bleeding, and high
susceptibility to infections & easily fatigued.
During complications of poor glucose control
visual impairment, neurologic symptoms such as
numbness, diziness, weakness, chest pain, GI
symptoms, genito-urinary symptoms.


Diagnostic Criteria

Normal
Impaired
Fasting
Diabetes
Mellitus
Fasting
Glucose
<110 mg/dl
110- 126
mg/dl
>= 120
mg/dl
2 hr post
prandial
plasma
glucose
<140 mg/dl
140 200
mg/dl
>= 200
mg/dl
OGTT
Plasma
glucose at
2 hr >= 200
mg/dl
Complications of DM

Site Presentation
Eyes Retionopathy, cataracts, blindness.
Kidney Neuropathy, Renal failure
Nervous system
Sensory: Peripheral neuropathy, cranial
neuropathy affecting cranial nerves III, IV, VI
& VII.
Autonomic: Gastroparesis, changes in
cardiac rate rhythm & dysfunction ; postural
hypotension ; GI neuropathy; urinary bladder
atony ; impotence.
Skin and oral mucosa Unusal infections, delayed wound healing
Periodontium Gingivitis and periodontal diseases
Cardio vascular system
Macro vascular diseases( accelerated
atherosclerosis) leading to peripheral
vascular diseases, coronary artery disease
and cerebro- vascular disease, ischeamic
ulcers, gangrenous feet.
Management
Primary treatment goals for DM are achieving
bld. glucose levels that are as close to normal as
possible & prevention of diabetic complications.
Diet, exercise, wt. control and medications are
mainstays of diabetic care.
Primary medications used in Type I DM is
Insulin.
Type 2 individuals frequently take oral
medications; & often use insulin to improve
glycemic control.
Oral hypoglycemic agents
Agent Generic name
Sulfonylurea/ 1
st

generation
Chlorpropamide, Tolazamide,
Tolbutamide, acetohexamide,
Sulfonylurea/ 2
nd

generation
Glyburide, glipizide,
glimeperide
Meglitinides
Repaglinide, Nateglinide
Biguanide
Metformin
Thiazolidinediones
Rosiglitazone, pioglitazone
A glucosidase inhibitors.
Acarbose, miglitol
Oral manifestations of DM

Mucosal conditions : oral dysesthesia including burning
mouth, altered wound healing , increase incidence of
infection and candidial infections (particularly acute
pseudomembranous candidiasis of the tongue, buccal
mucosa, gingiva.
Xerostomia (mostly side effect of OHA) and bilateral
generalised salivary gland enlargement or sialadenitis.
Dry mucosal surfaces caused by insufficient salivary
output are easily irritated, causing minor mucosal
ulcerations, oral burning sensations, increased
likelihood of fungal infections.


High incidence and severity of dental caries in DM
patients have been associated with xerostomia,
increased GCF glucose levels, increase in dental
plaque accumulation.
Prevalence and severity of gingivitis, periodontitis
and gingival inflammation, alteration of periodontal
wound healing.
Vascular changes seen in retina, glomerulus are
also seen in periodontium.
Progressive destructive periodontitis is more
common in patients with poor glycemic control.
Poor oral hygiene and smoking contribute to
the ^ incidence & severity of periodontitis in DM.



General Management Considerations

Access level of glycemic control.
Refer patients with signs and symptoms suggestive of
undiagnosed or uncontrolled DM to physicians for
diagnosis and treatment.
Obtain medical consultation if systemic complications
are present.
Use a glucometer to help avoid emergencies related to
diabetes.
Treat aggressively acute oral infections.
Place patients on frequent recall visits to monitor and
treat oral complications and maintain optimal oral
hygiene and diet.
Appointment scheduling
Appointment scheduling is determined by the
individuals medication regimen.
Traditionally it was recommended that medically
complex patients, including those with DM
receive dental treatment in morning to reduce
stress.
But it may not be true for some patients as the
release of endogenous epinephrine from stress
can have a counter-regulatory effect on the action
of insulin, leading to hyperglycemia.
Thus, the dentist must review with the patient the
diabetes medications, foods & fluids taken before
dental procedures.
The main factor to consider in determining
appt. times is the peak action of insulin and
the amt. of glucose being absorbed from the
gut following the last food intake.
The best time for dental Rx before / after
periods of peak insulin activity. This reduces
risk of peri-operative hypoglycemic reactions
which occur most often during peak insulin
activity.

Drug Peak Activity
Lispro insulin
30-90 mins.
Regular insulin
2-3 hrs.
NPH / Lente insulin
4-10 hrs.
Oral Sulfonylureas
Depends on individual
drug taken.
Specific Management Guidelines
Use of Epinephrine: Stress epinephrine and cortisol
production increases Bld. Glucose level increases. So,
pain control and stress reduction are essential.
Epinephrine is not contraindicated in these patients as it
helps promote better dental anaesthesia and significantly
lowers amounts of endogenous epinephrine released.
Oral Candidiasis : Signifies uncontrolled DM & can
manifest in presence of salivary hypofunction. Treatment
is similar except that topical antifungal medications should
be sugar free. If topical antifungal therapy is not
successful after 7 10 days, systemic antifungal agents
may be required.
Management of Recurrent HSV Infection: Oral
Acyclovir, famciclovir, or valacyclovir can be used.
Management of Burning moth syndrome: Xerostomia
and Candidiasis can contribute to the symptoms
associated with burning mouth. Amitriptyline can be
used.
Surgical considerations : Well controlled DM patient
= Normal patient. Antibiotics may be given for
orofacial infections and oral surgical procedures in
poorly controlled DM patient.
Periodontal Management: Nonsurgical debridement
and systemic antibiotics(tetracycline, doxycycline) is
the treatment.
Oral diseases management with Corticosteroids:
They increase glucose levels so physician should be
consulted and adjustment of dosage of drugs is
required.
Managing Diabetic
Emergency(Hypoglycemic Shock)
Hypoglycemia is a potentially life threatening
situation.
Signs and symptoms: Confusion, sweating,
tremors, agitation, anxiety, diziness, tingling or
numbness, and tachycardia. Seizure or loss of
consciousness may occur.
Bld. Glucose is checked with glucometer(15 sec)
and glucose is administerd to patient. Patient
recovers within 10-15 minutes and is observed for
30 to 60 mins.
Hyperglycemia is less likely to occur and
develops more slowly. Emergency medical
system is activated, opening of airway and
administration of O
2.
Factors that increase risk of
Hypoglycemia
Skipping or delaying food intake.
Injection of too much insulin.
Injection of insulin into tissue with high bld. flow.
Increasing exercise level without adjusting insulin or
sulfonylurea dose.
Alcohol consumption.
Inability to recognise symptoms of hypoglycemia.
Anxiety, stress.
Denial of warning signs or symptoms.
Past history of hypoglycemia.
Hypoglycemia unawareness.
Treatment of Hypoglycemia in dental
office.
Patient Condition Treatment
Patient is awake and able to
take food by mouth.
Give 15 gm oral carbohydrate.
125 -175 ml fruit juice or soda.
3-4 tablespoon sugar.
Hard candy.
Cake frosting.
Patient is unable to take
food by mouth and IV line is
in place.
Give 25-30 ml D50 (50 %
dextrose solution) or 1 mg
glucagon.
Patient is unable to take
food by mouth and IV line is
not in place.
Give 1 mg glucagon
Subcutaneously or IM at
almost any body site.
References
Burkets Oral Medicine (11
th
edition).
Thank you